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Biology subjects

Yeomans, D. C.

Publications and source records attributed to Yeomans, D. C..

3 recordsLinked to original sources

Core Coefficient quantifies transcription-factor functional dominance for therapeutic target selection

Transcription factors (TFs) operate in regulatory networks to control gene expression. The functional importance or leverage of a TF depends on the specific regulatory network in which it operates. Commonly used measurements of TF biology do not quantify the functional importance of TFs in these networks, which makes target selection for therapeutic intervention suboptimal. We developed the Core Coefficient (CC), a graph theory measure of TF functional dominance to overcome this limitation. Analysis of networks constructed from patient-biopsy and human post-mortem datasets revealed that these regulatory networks are organized in a functional hierarchy that is dominated by an identifiable and limited group of TFs, which we refer to as the Core. Analysis also revealed that the functional dominance of a TF, or the capacity to influence a cellular outcome, is a property of its position in the network hierarchy rather than its identity. While the Core consists of a group of functionally dominant TFs that control the network, the individual TFs forming that Core vary with cell type and cellular state. During the course of a given disease, from cancer to neurodegeneration, the functional dominance of TFs relevant to that disease shifts from low hierarchical importance to Core positions, whereas the functional dominance of other TFs is reduced or unchanged. CC can measure this shift in functional dominance and predict Core membership as a disease progresses. From a therapeutic standpoint, CC can also track the alterations in network hierarchy in diseased cells produced by treatments in the clinic. For example, network analyses of cancer cells before and after treatment from the same patients show dominant Core regulators shift from positions of high importance to positions of low importance after treatment. Experimental testing of these network mechanics in cancer cell lines showed CC can predict Core re-composition, signaling pathway reorganization and the cellular outcome of blocking a specific TF. In contrast, differential TF expression was informative in individual cases in these experiments but did not provide a general rule for measuring TF functional importance. This body of work introduces the CC, which quantifies TF functional dominance and enables the identification of targets for reprogramming TF networks to achieve a therapeutic objective.

systems biology↗

Noninvasive Diagnostic Ultrasound-Guided Focused Ultrasound Enables Selective, Reversible Inhibition of Peripheral Nociceptive Fibers and Prevents Acute Pain

BackgroundAcute postoperative pain remains a major clinical therapeutic challenge. Current peripheral nerve blockade (PNB) techniques are effective for some patients but are limited by invasiveness, short duration, reliance on highly trained providers, and off-target motor and sensory effects. Focused ultrasound (FUS) is a novel neuromodulatory technology with the potential to achieve noninvasive, selective, reversible, and prolonged inhibition of peripheral nociceptive fibers to prevent and treat acute pain. We hypothesized that noninvasive transcutaneous targeting of the rat sciatic nerve using co-aligned diagnostic ultrasound (dUS) and FUS transducers could produce selective and reversible inhibition of nociceptive pain behaviors while preserving motor and non-nociceptive sensory functions. MethodsIn an in vivo rat hindpaw incisional (HPI) pain model, using a novel, transcutaneous dUS-guided FUS system, the sciatic nerve was located with dUS, and FUS energy was applied to it just prior to hindpaw incision. FUS parameters were iteratively adjusted to achieve reversible, selective inhibition of nociceptive behaviors without changing motor and non-pain sensory behaviors. Animals were randomized into six groups: No Intervention (Control), HPI Only (Disease Control), Sham FUS, FUS Only, FUS+HPI (Intervention), and LA+HPI (Positive Control). Primary outcomes were changes in nociceptive sensory functions, assessed by thermal and mechanical sensitivity. Secondary outcomes were changes in non-nociceptive sensory and motor functions, assessed by hindpaw flexion and extension reflexes. ResultsCompared with the HPI Only group, the FUS+HPI group demonstrated (1) significant attenuation of hindpaw thermal hypersensitivity from day 0 - week 5.0 and week 8.0 - 16.0 (p < 0.05-0.001); (2) significant attenuation of mechanical hypersensitivity from day 0 until week 4.0 (p < 0.05-0.001); (3) no significant attenuation of flexion; and (4) no significant attenuation of extension. ConclusionsTranscutaneous dUS-guided FUS enables selective, reversible inhibition of A{delta} and C nociceptive fiber mediated behaviors while sparing A motor and A{beta} sensory behaviors. FUS-induced PNB prevented both acute and persistent pain behaviors. These findings support FUS as a promising noninvasive peripheral nerve blockade strategy for acute pain management.

neuroscience↗

Discovery of a Selective, State-Independent Inhibitor of NaV1.7 by Modification of Guanidinium Toxins

The voltage-gated sodium channel isoform NaV1.7 is highly expressed in small diameter dorsal root ganglion neurons and is obligatory for nociceptive signal transmission. Genetic gain-of-function and loss-of-function NaV1.7 mutations have been identified in select individuals, and are associated with episodic extreme pain disorders and insensitivity to pain, respectively. These findings implicate NaV1.7 as a key pharmacotherapeutic target for the treatment of pain. While several small molecules targeting NaV1.7 have been advanced to clinical development, no NaV1.7-selective compound has shown convincing efficacy in clinical pain applications. Here we describe the discovery and characterization of ST-2262, a NaV1.7 inhibitor that blocks the extracellular vestibule of the channel with an IC50 of 72 nM and greater than 200-fold selectivity over off-target sodium channel isoforms, NaV1.1-1.6 and NaV1.8. In contrast to other NaV1.7 inhibitors that preferentially inhibit the inactivated state of the channel, ST-2262 is equipotent against resting and inactivated protein conformers. In a non-human primate model, animals treated with ST-2262 exhibit markedly reduced sensitivity to noxious heat. These findings establish the extracellular vestibule of the sodium channel as a viable receptor site for selective ligand design and provide insight into the pharmacology of state-independent inhibition of NaV1.7. Significance StatementPain is among the most common reasons for seeking medical care, yet many frequently prescribed drugs, particularly the opioids, cause problematic side effects and carry a risk of addiction. Voltage-gated sodium ion channels (NaVs) have emerged as promising targets for the development of non-opioid pain medicines. NaVs are involved in the propagation of electrical signals along neurons throughout the body. Humans born without a functional copy of one sodium channel subtype, NaV1.7, are unable to experience most types of pain. In the present work, we disclose the discovery and characterization of a selective inhibitor of NaV1.7 that reduces sensitivity to a painful thermal stimulus in non-human primates. Findings from this work may help guide the development of novel, non-addictive drug candidates as alternatives to opioids.

neuroscience↗